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Research Article

The herpes simplex virus type 1 early gene (thymidine kinase) promoter is activated in neurons of brain, but not trigeminal ganglia, of transgenic mice in the absence of viral proteins

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Pages 116-122 | Published online: 10 Jul 2009
 

Abstract

Latent infection of sensory neurons and reactivation are necessary for maintenance of herpes simplex virus type 1 (HSV-1) in its host population. It has been proposed that the HSV-1 early gene, thymidine kinase (TK), may play an important regulatory role in this process. The authors used reporter transgenic mice to test whether sensory ganglia neurons could activate the HSV-1 TK reporter transgene in the absence of viral proteins. The reporter transgene was activated in subsets of neurons in the brain but was not activated in sensory ganglia neurons following a variety of experimental manipulations. These results do not support a role for TK in regulation of the latent viral genome.

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